In Rare Cases, Sarcoidosis Patients May Develop Psoriasis-like Plaques in Existing Lesions, Report Shows

Inês Martins, PhD avatar

by Inês Martins, PhD |

Share this article:

Share article via email
Psoriasis-like plaques on sarcoidosis

Psoriasiform lesions are a rare but established manifestation of sarcoidosis, in which psoriasis plaques are formed within sarcoidosis skin lesions. In a recent study, researchers at Thomas Jefferson University in Philadelphia and the University of Miami in Florida presented a case report of a patient with psoriasiform sarcoidosis, and discussed the possible role of tumor necrosis factor (TNF)-α in the appearance of this manifestation in sarcoidosis patients.

Their study, “Psoriasiform Sarcoidosis: Collision of Two Entities or Expression of One Common Pathogenesis?” was published in The Journal of Clinical and Aesthetic Dermatology.

The classic pathological finding of sarcoidosis is noncaseating granuloma, which consists of organized collections of inflammatory cells and epithelioid cells. Although sarcoidosis is most commonly found in the lungs and intrathoracic lymph nodes, other organs, such as the skin, eyes, liver, heart, and brain, may also be affected.

Approximately 25 percent of sarcoidosis patients have skin granulomas, 0.9 percent of which develop scaly skin lesion that resemble those seen in psoriasis. These lesions are most common in dark-skinned patients and generally seen on the legs.

The team reported the case of a 60-year-old African-American woman with a history of sarcoidosis, showing groundglass opacities with fibrotic changes and bilateral hilar and mediastinal lymphadenopathy in computed tomography (CT), as well as a compromised lung function.

When was patient was examined, she had a six-month history of cutaneous lesions in her lower legs and face. Although she had no history of psoriasis, a biopsy of her leg lesions showed non-caseating epithelioid granulomas with characteristics that led to the diagnosis of psoriasiform sarcoidosis.

The patient’s cheek lesion was injected with the cortiscosteroid triamcinolone, but the therapy had a poor response and the patient declined further treatment. Therefore, topical triamcinolone was prescribed, which induced some improvement.

Although the causes of sarcoidosis are not yet known, the immune response found in these patients has been widely studied. The inflammatory profile of sarcoidosis is characterized by the expression of inflammatory molecules, such as interleukin (IL)-12, interferon gamma (IFN-γ), and TNF-α, among others, that are responsible for the formation of the granulomas. Similarly, IFN-γ, TNF-α, and IL-12 are also expressed in psoriasis patients.

TNF-α is thought to have a crucial role in both diseases. In patients who remain symptomatic after taking steroids or other drugs to manage their sarcoidosis, TNF-α inhibitors, such as Thalomid (thalidomide), Remicade (infliximab), and Humira (adalimumab), have shown some benefit.

This suggests that TNF-α plays a key role in the development of sarcoidosis. Although further studies are required to explore the role of  TNF-α in the appearance of psoriasiform sarcoidosis, some authors have hypothesized that co-expression of TNF-α in both diseases may explain this manifestation in sarcoidosis patients.